It is widely established that BCG is an effective treatment for transitional cell carcinoma (TCC). Its clinical benefit might be attributable to effects both on immuno-competent cells themselves and the tumour, e.g., the induction of MHC Class II and ICAM-1 expression which are known to facilitate effector cell/ target cell interactions. It is of interest that the success of this therapy might be due in part to the induction of B7 molecules which could provide vital co-stimulatory signals to the host immune system. We showed that a panel of 8 TCC cell lines failed to express B7-1,-2,-3 molecules constitutively or after stimulation. Bladder cancer cells shed following immunotherapy also failed to express B7. After therapy B7 expression, however, was found on cells of lymphocytic and monocytic lineage produced locally. Of other co-stimulatory molecules examined (ICAM-3, HSP72, CD1b, VCAM) only CD40 appeared to be expressed on some of TCC cell lines. All cell lines failed to express previously predicted ICAM-3 indicating a possible existence of a novel ligand for LFA-1.

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